Hepatocarcinoma progression implies marked alterations of the tumor microenvironment that in turn enhance the malignant behavior by facilitating proliferation, migration and spread of cancer cells.An important mediator in this microenvironment is TGFβ, whose circulating level significantly increases cancer cell invasion and metastasis, and is often associated with the rate of cancer progression.However, the TGFβ-signaling network among hepatoeytes and stromal cell targets including fibroblasts, sinusoidal endothelial and inflammatory cells, is beginning to be unveiled.Mounting evidence indicates that interfering with TGFβ activity might be a molecular therapeutic option to pursue.More level of complexity is provided by myofibroblasts that are recruited into the avascular growth stage of developing hepatic micrometastasis and also undergo TGFβ-mediated effects.